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Virus linked to spread of breast cancer
and lymphoma
ANN ARBOR, MI - Feb. 28, 2001 -- Scientists
have found a link between the virus that causes the "kissing
disease" and aggressive forms of breast and immune system
cancers.
In a paper published in the March 2001 issue
of Nature Medicine, a team of scientists led by Dr. Erle
Robertson, of the University of Michigan's Cancer Center, show
how the Epstein-Barr virus that causes infectious mononucleosis
alters the function of a cellular protein that normally suppresses
the movement of malignant cells. When this natural brake on cell
migration is disabled by the virus, cancerous breast and lymphatic
cells are free to metastasize or spread.
"The Epstein-Barr virus is associated
with many human cancers -- including Burkitt's lymphoma, nasopharyngeal
carcinoma, Hodgkin's disease and invasive breast cancer,"
says Robertson in a prepared statement.
"This is the first evidence of a human
virus associated with the development of cancerous tumors targeting
a cellular protein to promote the migration of malignant cells,"
says Robertson who is an assistant professor of microbiology
and immunology at the U-M's Comprehensive Cancer Center.
| The virus is very common. More
than 90 percent of adults show signs of previous viral infection.
Adolescents infected with the acute phase of the virus can develop
infectious mononucleosis, but usually the body's natural |
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immune response forces the virus to revert
to its latent phase -- where it hides inside the nucleus of immune
cells called lymphocytes without producing any symptoms.
Even though the virus is endemic in humans,
Robertson emphasizes that most cells infected by the virus may
never become malignant. Additional genetic factors are required
to trigger development of cancer. Should cancer develop, however,
Robertson says the risk of metastasis may be higher in individuals
previously exposed to the virus.
"People with aggressive forms of cancer
are most vulnerable and should be checked to determine the status
of previous viral exposure when physicians are choosing the most
appropriate treatment for them," Robertson says. "It
also would be wise to closely monitor people with a history of
active Epstein-Barr viral infection for early signs of cancer."
In the study, Dr. Chitra Subramanian, a research
fellow, and Murray A. Cotter, a graduate student, investigated
a gene from the Epstein-Barr virus the protein produced by infected
lymphocytes when the viral gene produces its protein. The protein
was found in all EBV-infected cancerous lymphocytes in the breast
cancer and lymphoma cell lines analyzed in the study.
The researchers discovered that the viral
protein binds to a human protein, called Nm23-H1, found in all
human cells, which suppresses metastasis or the spread of malignant
cells.
"The interaction between the two proteins
disables Nm23-H1's natural ability to keep malignant cells in
their original location thereby promoting metastasis," explains
Robertson.
"We have mapped the binding site to one
region of the viral protein and hope in future research to identify
the exact location on the targeted protein," Robertson says.
"Our goal is to find the binding site and discover how to
block the interaction between these two proteins.
"If we succeed, physicians could one
day be able to treat primary breast and lymphatic cancers, as
well as other cancers associated with the Epstein-Barr virus,
without worrying about malignant cells spreading to other parts
of the body."
The research was funded by the Leukemia and
Lymphoma Society of America and the National Cancer Institute.
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